We still do not know for
certain how EDTA chelation therapy benefits atherosclerosis and other
age-related diseases. We only know that it binds to metallic ions in the
body. EDTA rapidly removes bound ionic metals via urinary excretion, and in the
process it also redistributes many metals within in the body. We have many
theories attempting to explain how EDTA reverses symptoms, improves
cardiovascular function, enhances quality of life, and improves blood flow,
but we still do not know the most important mechanism(s) of action.

A recent study by Frustaci and
associates in Italy showed that nutritional trace elements accumulate to
potentially toxic levels in diseased myocardium.1 Marked
increases in intracellular concentrations of myocardial trace
elements were measured by neutron activation analysis in separate groups of
patients with ischemia, valvular heart disease and idiopathic cardiomyopathy. The
nutritional elements, iron, zinc, chromium and cobalt increased from three-
to seven-fold in compromised myocardium. Metallic elements become toxic at
increased levels of that magnitude.

In patients with advanced
valvular disease and idiopathic cardiomyopathy, intracellular metals
increased to a similar extent as in those with ischemic coronary heart
disease.

Antimony and mercury also elevated to quite high levels. With no know
exposure to antimony or mercury, technical is a possibility. If these
findings are confirmed, this study is extremely important and should have
priority for further investigation.

In another study, copper and zinc accumulations in the brain were implicated in Alzheimer’s syndrome.
Alzheimer's researchers at the Massachusetts General Hospital reported
that buildup of copper and zinc in the brain causes the same type of protein
deposits that are a hallmark of Alzheimer's syndrome.2 Using
a strain of mice especially bred to develop a form of Alzheimer's, they found that a metal chelator, clioquinol,
neutralized those metals and reduced by half the formation of neurofibrillatory tangles and accumulations of beta-amyloid.
Unfortunately, clioquinol is much too toxic for use in humans.

Beta-amyloid protein in the
brain was found to trap copper. This bound copper catalyzed the release of
hydrogen peroxide, causing further neurological damage. Accumulations of
zinc in the brain acted to create a vicious cycle of increasing beta-amyloid, trapping more copper, leading
then to progressively more cell damage.

Nutritional trace elements
have a very narrow margin between physiologic and toxic levels. As shown in
Table I above, zinc rises to potentially toxic levels in the diseased heart.
Chromium and cobalt accumulate even more. It seems likely that other
nutritional elements not yet measured might accumulate to a similar extent.
Iron accumulates to toxic levels and also acts as a catalyst to
speed the production of damaging free oxygen radicals.

We must carefully consider
this recent evidence indicating that EDTA benefits patients, at least in
part, by removing abnormal accumulations of essential nutritional trace
elements from diseased organs and arterial walls.

EDTA in the body remains
extracellular, and can only remove intracellular accumulations of metallic
ions by first binding and removing elements outside of cells. That process
establishes a concentration gradient, which draws
unwanted intracellular metals out through cell walls. Only then can they be chelated. That is one reason why EDTA is administered slowly, over several
hours. Diffusion outward is a relatively passive process and occurs much
more slowly than the subsequent binding by EDTA. That may also be the reason
why no data have been published showing improved blood flow using oral EDTA.
Absorption of oral EDTA is minimal and slow, and resulting plasma
concentrations are much lower than achieved by the intravenous route,
resulting in a much weaker intracellular to extracellular concentration
gradient.

Based on recent findings, it
now appears that an important mechanism of action of EDTA chelation
therapy is to restore safe and desirable levels of essential nutritional
metallic elements in compromised cells. Urinary
excretion of metallic toxins and free radical catalysts might be only a
secondary benefit.